In animal studies at least, exercises increases brain derived neurotrophic
factor in the hippocampus though I suspect there is an overall benefit for
the CNS.
As to ssris and neurogenesis, my spin on that is as serotonin levels rise
the HPA axis is modified reducing cortisol levels, the dentate gyrus is very
high in GC receptors and neural progenitor cells v. sensitive to
glucocorticoids. Thus the delay in ssri efficacy may relate to this slow
turning down of excessive cortisol production, which is one of the most
frequently reported aspects of depression. Enriched environment is worth
looking at, but make sure it is not one that raises stress for the child!
One reason I would be opposed to giving SSRIs to children is that I have
noted some reports that in animals studies the administration of the same in
infancy can result in the animal, in adulthood, developing behavioural and
neurologic characteristics similiar to that observed in depression. I'm
still tracking for references on this though so if anyone can help ... .
John..
--
johnYYYcoe at tpg.com.au
remove YYY in reply
"Matthew Kirkcaldie" <Matthew.Kirkcaldie at newcastle.edu.au> wrote in message
news:Matthew.Kirkcaldie-BD35FF.15445105092003 at seagoon.newcastle.edu.au...
> Hi Gregg,
>> By coincidence, I am currently grappling with some of the issues raised
> by neurogenesis and antidepressants. The short answer to your question
> is that the neurogenesis (NG) angle isn't a good argument for giving
> Prozac to developmentally delayed children.
>> There are two main reasons: one is that the cells which migrate to the
> olfactory bulbs are generated in the subventricular zone - the ones
> generated in the hippocampus stay in the hippocampus, and they are the
> ones increased by Prozac. So Prozac wouldn't increase cells going to
> the olfactory bulbs.
>> The other reason, which is more a hypothesis of mine, is that the extra
> NG we see from antidepressants is the result of their activity being
> integrated into behaviour - i.e. the antidepressants make large changes
> to the monoamine systems "out there" in the brain, but before these
> changes play a part in behaviour, they have to be integrated with the
> rest of the brain's activity. Gerd Kempermann had the idea that NG is
> related to the hippocampus getting used to a new setup - so I want to
> extrapolate that idea to suggest that antidepressant-enhanced NG is a
> mark of the brain adjusting to the large changes caused elsewhere by the
> drug, and not the direct agent of those changes.
>> So I think neurogenesis in the hippocampus is more about behavioural
> flexibility rather than having "more brain" or developing faster. The
> cells die at the same rate new ones are generated - it's just that the
> new ones can grow into new patterns more easily than the old ones could
> be adapted.
>> Interestingly, you can enhance neurogenesis by exposing an individual to
> an enriched environment (lots of interesting things to see, hear, touch,
> taste and smell). As a parent who's obviously reading widely and
> seeking knowledge, it sounds like you are already likely to be doing
> that sort of thing anyway! I wouldn't be messing with kids' serotonin
> systems as a rule, especially kids who are maturing more slowly than the
> norm.
>> Hope that helps. As an aside, I was disappointed to see the focus of
> that Sci Am issue was "improving the brain". Every shred of evidence we
> have is that the brain organises itself optimally to use its resources
> and its potential to the fullest - it seems like fallacy of the worst
> kind to think that we could just "stimulate" or "tune" something and
> augment its powers. If it were that simple, don't you think we'd
> already be doing it?
>> Regards,
>> Matthew.
